The chief aim of these experiments is to determine the maximum range of sarcomere lengths over which intact cardiac muscle can shorten and generate force and then to investigate the mechanism which dynamically alters that range. The methods entail controlling the sequence of contractile force and sarcomere length changes - the latter measured by light diffraction - in isolated strips of heart muscle. First, I will investigate how sarcomere length and sarcomere shortening are modified by the superimposed mechanical conditions. Specifically I will determine whether myofilament sliding interrupts mechanical activity, thereby limiting the sarcomere length operating range. A principal goal will be to quantify the deactivating response to myofilament displacement so that its dependence on the level of myofibrillar activity can be determined. Another experimental goal is to determine if the rate of calcium binding and uptake by the sarcoplasmic reticulum actually controls the dynamics of relaxation in the absence of myofilament sliding. A third, ancillary project entails exploration of the results seen from the intact muscle experiments at the level of the single cell. Secondary aims of these experiments will be to: 1) measure the force-velocity relations of cardiac sarcomeres; 2) assess the influence of pericellular connections upon the sarcomere dynamics; and 3) evaluate the possibility that some inotropoic mechanisms increase the sarcomere length operating range by shifting the length dependence of tension (as opposed to simply elevating tension at respective sarcomere lengths).